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      Functional mechanism of Ginsenosides on tumor growth and metastasis

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          Abstract

          Ginsengs, has long been used as one medicinal herb in China for more than two thousand years. Many studies have shown that ginsengs have preventive and therapeutic roles for cancer, and play a good complementary role in cancer treatment. Ginsenosides, as most important constituents of ginseng, have been extensively investigated and emphasized in cancer chemoprevention and therapeutics. However, the functional mechanism of Ginsenosides on cancer is not well known. This review will focus on introducing the functional mechanisms of ginsenosides and their metabolites, which regulate signaling pathways related with tumor growth and metastasis. Ginsenosides inhibit tumor growth via upregulating tumor apoptosis, inducing tumor cell differentiation and targeting cancer stem cells. In addition, Ginsenosides regulate tumor microenvironment via suppressing tumor angiogenesis-related proteins and pathways. Structural modification of ginsenosides and their administration alone or combinations with other Chinese medicines or chemical medicines have recently been developed to be a new therapeutic strategy for cancer.

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          Ginsenosides as Anticancer Agents: In vitro and in vivo Activities, Structure–Activity Relationships, and Molecular Mechanisms of Action

          Conventional chemotherapeutic agents are often toxic not only to tumor cells but also to normal cells, limiting their therapeutic use in the clinic. Novel natural product anticancer compounds present an attractive alternative to synthetic compounds, based on their favorable safety and efficacy profiles. Several pre-clinical and clinical studies have demonstrated the anticancer potential of Panax ginseng, a widely used traditional Chinese medicine. The anti-tumor efficacy of ginseng is attributed mainly to the presence of saponins, known as ginsenosides. In this review, we focus on how ginsenosides exert their anticancer effects by modulation of diverse signaling pathways, including regulation of cell proliferation mediators (CDKs and cyclins), growth factors (c-myc, EGFR, and vascular endothelial growth factor), tumor suppressors (p53 and p21), oncogenes (MDM2), cell death mediators (Bcl-2, Bcl-xL, XIAP, caspases, and death receptors), inflammatory response molecules (NF-κB and COX-2), and protein kinases (JNK, Akt, and AMP-activated protein kinase). We also discuss the structure–activity relationship of various ginsenosides and their potentials in the treatment of various human cancers. In summary, recent advances in the discovery and evaluation of ginsenosides as cancer therapeutic agents support further pre-clinical and clinical development of these agents for the treatment of primary and metastatic tumors.
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            Calcium and ROS-mediated activation of transcription factors and TNF-alpha cytokine gene expression in macrophages exposed to ultrafine particles.

            Ultrafine (Uf) particles are a component of particulate air pollution suggested to be responsible for the health effects associated with elevations of this pollutant. We have previously suggested that Uf particles, through the induction of oxidative stress, may induce inflammation in the lung, thus exacerbating preexisting illness in susceptible individuals. Alveolar macrophages are considered to play a key role in particlemediated inflammation and lung disease. The effect of Uf particles on rat alveolar macrophages and human blood monocytes was investigated with reference to the roles of calcium and reactive oxygen species (ROS). TNF-alpha protein release, intracellular calcium concentration, TNF-alpha mRNA expression, and transcription factor activation were studied as end points after treatment of rat alveolar macrophages or peripheral blood monocytes. The calcium channel blocker verapamil, the intracellular calcium chelator BAPTA-AM, the calmodulin inhibitor W-7, and the antioxidants Trolox and Nacystelin (NAL) were included in combination with Uf particles. Verapamil reduced intracellular calcium concentration in rat alveolar macrophages on stimulation with Uf particles. This effect was also apparent with transcription factor AP-1 activation. All antagonists and antioxidants reduced Uf-stimulated nuclear localization of the p50 and p65 subunits of NF-kappaB in human monocytes. Verapamil, BAPTA-AM, and NAL reduced Uf-stimulated TNF-alpha protein release, whereas only verapamil reduced Uf-stimulated mRNA expression in rat alveolar macrophages. In human monocytes, verapamil, Trolox, BAPTA-AM, and W-7 reduced Uf-stimulated TNF-alpha protein release. These findings suggest that Uf particles may exert proinflammatory effects by modulating intracellular calcium concentrations, activation of transcription factors, and cytokine production through a ROS-mediated mechanism.
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              American ginseng: potential structure-function relationship in cancer chemoprevention.

              Ginseng has a prominent position on the list of best-selling herbal products in the world, and its main active constituents are thought to be ginsenosides. Compared with the long history of use and widespread research on Asian ginseng, studies of American ginseng are relatively limited, especially regarding cancer chemoprevention. In recent studies of American ginseng, steaming or heating altered the ginsenoside profile and thereby increased anticancer effects. Yet the ginsenoside structures and their activities have not been systematically elucidated. In this commentary, we introduce the different ginsenosides in American ginseng, both the naturally occurring compounds and those resulting from steaming or biotransformation. We briefly review American ginseng's reported anticancer effects and their mechanisms of action, and explore the possible structural-function relationship with a focus on sugar molecules, hydroxyl groups and stereoselectivity in ginsenosides. Understanding these relationships may produce insights into chemical and pharmacological approaches for enhancing the chemopreventive effects of ginsenoside and for developing novel anticancer agents. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Saudi J Biol Sci
                Saudi J Biol Sci
                Saudi Journal of Biological Sciences
                Elsevier
                1319-562X
                2213-7106
                02 February 2018
                July 2018
                02 February 2018
                : 25
                : 5
                : 917-922
                Affiliations
                [a ]Department of Pharmacy, Changchun University of Chinese Medicine, Changchun, Jilin, PR China
                [b ]National Cancer Institute, National Institutes of Health, Frederick, MD, USA
                Author notes
                [* ]Corresponding authors at: Department of Pharmacy, Changchun University of Chinese Medicine, 1035 Boshuo Road, Changchun, Jilin 130117, PR China (Z. Qiu). National Cancer Institute, 1050 Boyles St., Bldg 560, Rm 12-34, Frederick, MD 21702, USA (P. Qu). qzdcczy@ 123456163.com peng.qu@ 123456nih.gov
                Article
                S1319-562X(18)30021-4
                10.1016/j.sjbs.2018.01.012
                6087812
                30108441
                a5cf54f7-5881-44c2-99fd-457b8b501b8b

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 15 January 2018
                : 18 January 2018
                Categories
                Article

                functional mechanism,ginsenosides,tumor growth,tumor metastasis

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